Literature DB >> 683464

Pathogenesis of longitudinal splitting of muscle fibres in neurogenic disorders and in polymyositis.

M Swash, M S Schwartz, M K Sargeant.   

Abstract

Longitudinal splitting of muscle fibres has been studied in the biopsies of eighteen patients with neurogenic disorders, and of twenty with polymyositis. In neurogenic disorders splitting predominantly affects hypertrophied fibres, and is probably due to mechanical overload induced by normal loads imposed on a weakened muscle. A similar phenomenon occurs in hypertrophied fibres in chronic polymyositis. However, in acute, or active polymyositis an appearance resembling fibre splitting can result from sequestration of necrotic segments within a fibre and also from regeneration occurring within intact sarcolemmal tubes after segmental sub-endomysial necrosis. These different processes, which can be distinguished by light and ultrastructural criteria, are important compensatory factors in neuromuscular disorders.

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Year:  1978        PMID: 683464     DOI: 10.1111/j.1365-2990.1978.tb00551.x

Source DB:  PubMed          Journal:  Neuropathol Appl Neurobiol        ISSN: 0305-1846            Impact factor:   8.090


  5 in total

1.  Teaching monograph: pathology of skeletal muscle diseases.

Authors:  U U DeGirolami; T W Smith
Journal:  Am J Pathol       Date:  1982-05       Impact factor: 4.307

2.  Muscle damage and repair in voluntarily running mice: strain and muscle differences.

Authors:  A Irintchev; A Wernig
Journal:  Cell Tissue Res       Date:  1987-09       Impact factor: 5.249

3.  Deficiency of the E3 ubiquitin ligase TRIM32 in mice leads to a myopathy with a neurogenic component.

Authors:  Elena Kudryashova; Jun Wu; Leif A Havton; Melissa J Spencer
Journal:  Hum Mol Genet       Date:  2009-01-19       Impact factor: 6.150

4.  Origin and significance of small muscle fibres in neuromuscular disease.

Authors:  L M Tang; M Swash
Journal:  Virchows Arch A Pathol Anat Histopathol       Date:  1986

5.  Satellite cells fail to contribute to muscle repair but are functional in Pompe disease (glycogenosis type II).

Authors:  Lydie Lagalice; Julien Pichon; Eliot Gougeon; Salwa Soussi; Johan Deniaud; Mireille Ledevin; Virginie Maurier; Isabelle Leroux; Sylvie Durand; Carine Ciron; Francesca Franzoso; Laurence Dubreil; Thibaut Larcher; Karl Rouger; Marie-Anne Colle
Journal:  Acta Neuropathol Commun       Date:  2018-10-31       Impact factor: 7.801

  5 in total

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